Target intelligence / Profile preview

N-type voltage-gated calcium channel subunit alpha-1B (CaV2.2 (or α1B))

Target
CaV2.2 (or α1B)
Molecular classification
Ion channel, Voltage-gated calcium channel, Transmembrane protein
01

Overview

The N-type voltage-gated calcium channel subunit alpha-1B (CaV2.2, encoded by the CACNA1B gene) is the primary pore-forming subunit of the N-type calcium channel, a high-voltage-activated ion channel predominantly found in presynaptic nerve terminals and neuroendocrine cells. It is integral to synaptic transmission, controlling the entry of calcium ions into neurons to trigger neurotransmitter release. Structurally, the alpha-1B subunit forms a central pore surrounded by four homologous domains, each consisting of six transmembrane segments, and associates with several auxiliary subunits (α2δ, β, sometimes γ) to modulate function and expression. These channels play a key role in pain pathways and are pharmacologically targeted by peptide toxins and the drug ziconotide for severe chronic pain, with emerging research into their involvement in various neurological disorders[1][2][3][4][5][8].

Other names
Voltage-dependent N-type calcium channel subunit alpha-1BCaV2.2BIIIBrain calcium channel IIICACH5CACNL1A5Calcium channel, L type, alpha-1 polypeptide isoform 5CACNA1B (gene name)N-type calcium channel
02

Mechanism of action

Blockage of calcium influx into neuronal terminals; Inhibition of neurotransmitter release (especially pain neurotransmitters); Disruption of synaptic transmission in pain pathways[1][2]

03

Biological functions

Neurotransmitter releaseSignal transductionRegulation of synaptic transmissionPain signalingRegulation of calcium ion importModulation of gene expression, cell motility, division, and death[1][2][5][8]
04

Disease associations

Neurodegenerative diseaseCancer painNeuropathic painEpilepsy (investigational/experimental)Other neurological disorders involving synaptic dysfunction[1][2][8]
05

Safety considerations

CNS effects: Dizziness, confusion, hallucinations (notably with ziconotide)[1][2]Motor and autonomic dysfunction due to broad blockade of synaptic transmissionPotential cardiovascular effects if selectivity is lost
06

Interacting drugs

Ziconotide (FDA-approved, for refractory severe chronic pain)

2 more in the full profile.

07

Biomarkers

No widely established clinical biomarkers for patient selection; experimental work may assess gene or protein expression (e.g., CACNA1B mRNA in certain tissue contexts)[8]

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